Epigenetic Regulation in Drosophila Tumor Models

Abstract

This chapter investigates the role of epigenetic regulation in tumorigenesis using Drosophila melanogaster as a model organism. It underscores the advantages of Drosophila for studying epigenetic mechanisms in cancer and focuses on key epigenetic regulators, such as Polycomb and Trithorax complexes, which modulate chromatin structure and gene expression. The chapter explores the roles of these complexes in various Drosophila tissues, including imaginal discs, the central nervous system, and adult stem cells, emphasizing their context-dependent functions in both tumor suppression and promotion. It challenges the somatic mutation theory (SMT) of cancer by emphasizing theories and experimental results suggesting a major contribution of epigenetic mechanisms in cancer initiation and progression. The concept of tumor reversion through epigenetic reprogramming is introduced, suggesting that non-mutational changes can revert tumor cells to a benign state. The tissue organization field theory (TOFT) and the epigenetic progenitor hypothesis are discussed to explain the epigenetic origins of cancer. Significant data highlight the critical role of epigenetic regulation in maintaining cellular identity, preventing tumorigenesis, and contributing to cancer when dysregulated. The chapter discusses the potential for epigenetic therapies and the need for further research to unravel the complex interplay between genetic and epigenetic factors in cancer.

Keywords: Chromatin regulation; Epigenetic reprogramming; Epigenetic therapies; Epigenetics; Polycomb group; Trithorax group; Tumor reversion.